Many individuals with spinal cord injury cannot generate the muscle torque necessary for efficient locomotion even after extensive rehabilitation. This may be attributed to both neural and muscular declines after injury. However, the ability to step and stand can be reacquired by mammals even after a complete thoracic spinal cord transection by task specific training that maintains appropriate peripheral sensory inputs. This potential for neural plasticity may also exist in human lumbosacral neural circuits. Spinal cord injured patients who have no detectable voluntary motor control or sensation below the level of the lesion can generate step like efferent patterns when suspended over a moving treadmill belt with partial body weight support with manual assistance. Further, peripheral sensory modalities such as limb load, speed of locomotion, joint position and cycle period may modulate the EMG activity of extensors and flexors during stepping on the treadmill by interacting with lumbosacral neural circuits. Repetitive step training may have enduring effects on the capacity of these neural networks and has the potential to reduce the effects of muscle disuse. In the proposed experiments the Principal Investigator aims to determine 1) the responsiveness of the human lumbosacral spinal cord after a clinically complete thoracic injury to sensory inputs related to limb load, the kinematics of the phases of the step cycle, and hip position during stepping with body weight support on a moving treadmill. 2) whether training with these inputs can optimize the level of motor pool activity and increase muscle mass and therefore the potential for locomotion, the proposed studies will employ measures of kinematics, loading, and electromyographic activity of the lower limbs. The results will provide a better understanding of neural mechanisms that are available in the human spinal cord to generate locomotion and will facilitate the development of new rehabilitation strategies for optimizing the recovery of mobility following neurologic injury.